PATHOPHYSIOLOGY OF DIABETES MELLITUS TYPE II (NON-INSULIN DEPENDENT) WITH ITS MULTI ORGAN COMPLICATIONS

PREDISPOSING FACTORS

NON-MODIFIABLE FACTORS: MODIFIABLE FACTORS:

AGE- 69 YRS. OLD HISTORY OF HIGH FAT, HIGH CARBOHYDRATE DIET
HYPERTENSION SINCE 2000 SEDENTARY LIFESTYLE
OVERWEIGHT (BMI OF 28.04 M2/KG)

INCREASE INSULIN PRODUCTION

INSULIN RESISTANCE STARVATION OF CELLS POLYPHAGIA

POST PRANDIAL HYPERGLYCEMIA DEVELOPS

BETA CELLS EXPOSURE TO HIGH GLUCOSE ALPHA CELLS INCREASES

BECOMES LESS EFFICIENT
INSULIN, PIOZONE
INCREASE IN GLUCAGON
DECLINING INSULIN SECRETION
IN THE BETA CELLS INCREASE STIMULATION OF
GLUCOSE PRODUCTION
FROM LIVER (GLYCOGENOLYSIS)
DECREASE GLUCOSE UPTAKE

INCREASE SERUM GLUCOSE

FASTING HYPERGLYCEMIA IMBALANCED
NUTRITION

METABOLIC TOXICITY IN THE

HYPEROSMOLALITY OF BLOOD PLASMA
PANCREAS

SHIFT OF WATER FROM INTRACELLULAR PROFOUND CELLULAR

TO EXTRACELLULAR SPACE VOLUME DEPLETION
A B
THIRST FEELING (HYPOTHALAMUS) POLYDIPSIA

FAILURE TO PRODUCE INSULIN AND INSULIN STIMULATES LIVER TO BREAK DOWN

SUSTAINED ELEVATED BLOOD GLUCOSE GLUCAGON INTO OF
PRODUCTION FATTY ACIDS GLUCAGON
EXCESSIVE
RESISTANCE
 A FATTY PANCREATIC AND HEPATIC ATROPHY
B

DESENSITIZATION OF ABNORMAL FUNCTIONING FORMATION OF FATTY INFILTRATES

BETA CELLS OF ALPHA CELLS
DEVELOPMENT OF AMYLOID DEPOSIT IN ISLET
PRODUCTION OF
FAILURE TO PRODUCE INSULIN
EXCESSIVE GLUCAGON INCREASE OF OVERALL SIZE OF LIVER AND PANCREAS
AND INSULIN RESISTANCE

GLYCOGEN VACOULES PRESENT IN CELL NUCLEI

SUSTAINED ELEVATED INCREASE LIPOLYSIS
BLOOD GLUCOSE OF ADIPOSE TISSUE
LIVER DAMAGE
EXCESSIVE AMOUNTS OF VERY LOW DENSITY
ENZYME SYSTEMS CONVERT HYPERTRIGLYCERIDEMIA
FATTY ACIDS ARE MOBILIZED LIPOPROTEIN WILL BE
GLUCOSE TO OTHER SUGARS G
FROM ADIPOSE TISSUE CELLS SECRETED
SUCH AS SORBITOL AND FRUCTOSE
AND TRANSPORTED TO THE VERY LOW DENSITY
AS OF JUNE 15
LIVER LIPOPROTEINS WILL 2009
TRANSFER EXCESS  LDH – (313 –
ELECTROLYTE
SORBITOL, FRUCTOSE AND TRIGLYCERIDE TO HIGH 618 u/L) = 1098
FATTY ACYL COA IS IMBALANCE DENSITY LIPOPROTEIN u/L
GLUCOSE ACCUMULATE IN THE  AST - (0 – 38
BASEMENT MEMBRANE OF THE TRANSPORTED TO AND LOW DENSITY u/L) = 65.1
CELL AND BETWEEN CELLS MITOCHONDRIA FOR B- LIPOPROTEIN
OXIDATION
SIMVASTATIN
THICKENED BASEMENT
MEMBRANE OF CELLS TRIGLYCERIDE TRIGLYCERIDE
UNDERGOES DECARBOXYLATION 3-HYDROXYBUTARATE ENRICHED- HDL ENRICHED- LDL
DEHYDROGENASE
ACETONE PRODUCTION
C 3-HYDROXYBUTYRATE DISSOCIATE FROM TRIGLYCERIDE
APOPROTEIN.1 ENRICHED LDL WILL
BECOME SMALLER
DIABETIC AND DENSER THAN
FORMATION OF KETONE BODIES REDUCES THE
KETOACIDOSIS THE NORMAL LDL
TOTAL
CONCENTRATION
ACCUMULATION IN THE BLOOD OF HDL AVAILABLE
METABOLIC PENETRATION OF
ACIDOSIS FOR REVERSE
BLOOD VESSEL
CHOLESTEROL
K EXCRETION OF KETONES IN THE KIDNEYS TRANSPORT
K NaHCO3
D
F
E

IMPAIRED GAS EXCHANGE

 D
URINALYSIS AS OF JUNE 13
C KETONURIA
REVEALS 10MG/DL OF KETONES KUSSMAUL’S MACROVASCULAR
E F H
RESPIRATION COMPLICATIONS
CELLS RECEIVE INADEQUATE OXYGEN
ANDNUTRITION
DECREASED ATHEROSCLEROSIS
I
PCO2

INCREASED POLYOL INCREASED ACTIVATION INCREASED

FORMATION OF PROTEIN IMPAIRED
PATHWAY FLUX HEXOSAMINE
OF KINASE C GAS ACUTE CORONARY
PATHWAY
ADVANCE EXHANGE SYNDROME
ALDOSE
GLYCATION
REDUCTASE ALTERS BLOOD SUBSTRATES NON ST SEGMENT
END
CONVERTS FLOW AND ARE LINKED TO INEFFECTIVE MYOCARDIAL
ALDOHEXOSES TO CHANGES TRANSCRIPTION BREATHING INFARCTION
AGE BINDS TO
ITS RESPECTIVE ENDOTHELIAL FACTORS PATTERN
RECEPTORS OF
ALCOHOL ( POLYOL PERMEABILITY THROMBOEMBOLISM
MACROPHAGE
S RELEASING STIMULATES
EXCESSIVE CYTOKINES TRANSFORMATION PERIPHERAL ARTERIAL DISEASE
SORBITOL OF PROTEINS INTO
PRODUCTION VASCULAR CELL GROWTH FACTORS
PROLIFERATIO AND STROKE
N AND PLASMINOGEN
FUNCTION ARE ACTIVATOR CHEST X-RAY OF JUNE 13, 2009
REVEALED ATHEROSCLEROTIC AORTIC
I KNOB
MICROVASCULAR COMPLICATIONS

ACCUMULATION OF SORBITPOL TO RETINOPATHY NEUROLOGIC DYSFUNCTION

G
VASCULAR INTIMA
NEUROPATHY DECREASE IN PRODUCTION OF SERUM DECREASE ABSORPTION OF
ALBUMIN ALBUMIN IN THE GIT
H
DIABETIC NEPHROPATHY
K
J K
J
 LOW SERUM ALBUMIN (HYPOALBUMINEMIA)

GLOMERULAR BASEMENT
MEMBRANE THICKENS 6 EGG WHITES LOW ONCOTIC PRESSURE OF CAPILLARIES

CAPILLARY NARROWING INEFFECTIVE FLUID SHIFT FROM INTRAVASCULAR

TISSUE SPACE TO THE EXTRAVASCULAR SPACE
PERFUSION

DECREASE GLOMERULAR FILTRATION IMPAIRED URINARY BIPEDAL EDEMA GRADE 2

SURFACE AREA ELIMINATION

INCREASE PERMEABILITY TO BURINEX,

MACROMOLECULES
FLUID VOLUME EXCESS FUROSEMIDE

VASCULAR LEAKAGE
ELECTROLYTE
IMBALANCE
OSMOTIC
EFFECT OF GLUCOSE IN BLOOD IS BLOOD ALBUMIN
GLUCOSE EXCRETED IN URINE GOES TO URINE KALIUM DURULE,
(GLYCOSURIA) (ALBUMINURIA) SODIUM
POLYURIA BICARBONATE

URINALYSIS AS OF URINALYSIS AS OF
JUNE 13 JUNE 22 AND 25
REVEALED +1 Source: Medical Surgical Nursing by Black et. Al,
REVEALED ++++
Brunner and Suddarth’s Medical Surgical Nursing
SUGAR ALBUMIN
by Smeltzer et.al, Harrison’s Principle of internal
medicine, Medical Surgical Nursing by
Ignatavicius, Pathophysiology of diseases by
McPhee

INSULIN, PIOZONE